Deficiency diseases
Research into deficiency diseases in shrimp is limited compared with similar studies on finfishes (e.g. FAO, 1992a).
Vitamin deficiency
Rai and Reddy (2004) studied the effect of exclusion of individual water-soluble (thiamine, riboflavin, pyridoxine, cyanocobalamin, pantothenic acid, folic acid, niacin, biotin, choline, inositol and ascorbic acid) and fat-soluble vitamins (vitamins A, D, K and E) in semi-purified diets on growth and survival of juvenile P. monodon. Diets lacking riboflavin and vitamin K did not affect growth and survival of shrimp. Deletion of inositol and choline resulted in poor growth. Maximum growth was observed in the control diet supplemented with all vitamins. Diets deficient in ascorbic acid, biotin, folic acid, niacin, thiamine and alpha–tocopherol resulted in poor appetite and poorer feed conversion efficiency. All treatments except the control resulted in histological changes in the digestive gland cells, but changes were more severe in the treatment without a vitamin supplement followed by inositol, choline and ascorbic acid deficient diets.
Clinical signs of thiamin deficiency in shrimp species are anorexia, poor growth, increased mortality rates (lower survival) and higher FCRs (Chen, Wu and Tang, 1991).
A lack of vitamin C has been shown to cause black death disease in shrimp (Couch and Fournie, 1993). Juvenile shrimp develop large, black, necrotic foci in the gills, subcutis, and walls of the stomach and hindgut. Secondary infections by Vibrio spp. are common. This disease is not found if primary productivity (algal production) is present. Black death disease has not been observed in subadult and adult shrimp and is thus apparently confined to the juvenile stages of the species.
Black gill disease can also be caused by a lack of vitamin C (Jintoni, 2002).
Cramp tail syndrome
Another nutrition-related disease recognized in shrimp is cramped–tail syndrome (CTS) or cramped–muscle syndrome (CMS) (Couch and Fournie, 1993). CMS has been suggested to be caused by physiological or nutritional factors that are enhanced by physical or environmental stressors. Data suggest that reduced dietary and/or environmental potassium (relative to the cations Ca, Na and Mg) may be the principal factor in the etiology of CMS in penaeid shrimp. Partially cramped shrimps swim with a humped abdomen, whereas fully cramped individuals lie on their sides at the pond/tank bottom (Jintoni, 2002). Mortality can be reduced if shrimp are handled during cool weather (Liao and Chin, 1980). CTS appears to be caused by one or more of the following conditions:
- high temperature stress,
- vibriosis,
- mineral imbalances, and/or
- toxins in the water.
An acceptable level of CTS would be 5 percent or less (Clifford and Cook, 2002). However, even 5 percent is a high number, indicating some problem.
Soft-shell syndrome
Feed quality may also lead to a condition called soft-shell syndrome. Nutritional deficiency, pesticide contamination and poor pond water and soil condition have all been associated with this condition (Jintoni, 2002). Inadequate feeding practices such as improper feed storage, use of rancid or low-quality feeds and lack of supplementary feeding in ponds with relatively high stocking densities are associated with a high incidence of soft-shelling in P. monodon. The shell of affected animals is thin and persistently soft for several weeks. It is often dark, rough and wrinkled, and affected shrimp are weak. Normal shrimp that have moulted have a smooth, clean soft shell that hardens within 1–2 d.
Affected shrimp grow slowly and eventually die. Water must be change immediately and frequently, particularly when pesticide contamination is suspected.
Blue disease or pigment deficiency syndrome
Blue disease, sky blue shrimp disease, blue-shell syndrome or pigment deficiency syndrome (PDS) is reported to be associated with low levels of the carotenoid astaxanthin in cultured Penaeus monodon. A diet containing 50 ppm of astaxanthin fed over four weeks restored normal greenish-brown pigmentation in tiger prawns (Menasveta et al., 1993). The disease is observed in intensive culture systems toward the end of the growout culture period (Jintoni, 2002). It is also associated with bleaching of broodstock ovaries and reduced early larval performance in species such as Fenneropenaeus indicus (Regunathan and Wesley, 2006). Astaxanthin is also beneficial for the postlarval stages of the tiger prawn (Pan, Chien, and Cheng, 2001; Pan and Chien, 2004). Broodstock performance can be improved by feeding 30 g/kg Spirulina supplemented diet immediately after the appearance of clinical signs. Carotenoid content in commercially available Spirulina ranges from 3.5 to 5.7 g/kg.
Aflatoxin poisoning, “red disease”
The mould Aspergillus sp. is a common contaminant in prawn feeds and leads to aflatoxin in the food. This causes red disease or red discolouration. Check for old, rancid feeds and feeds stored in hot conditions. 50 µm of aflatoxin per gram of feed causes atrophy and necrosis of the hepatopancreas (Jintoni, 2002). The condition leads to gradual mortalities and losses of up to 98 percent in three months.
